Cystatin C is correlated with mortality in patients with and without acute kidney injury.

BACKGROUND: Recent research has shown cystatin C to predict mortality and cardiovascular morbidity independent of renal function. The aim of this study was to evaluate the prognostic value of cystatin C on mortality in adult general ICU patients with acute kidney injury (AKI). We later expanded the study and included patients without signs of AKI. METHODS: A total of 845 ICU patients were analysed for cystatin C and classified according to the RIFLE criteria. Of these, 271 patients with either creatinine >150 micromol/l, urea >25 or anuria/oliguria entered the AKI cohort. The remaining 562 patients entered the non-AKI cohort. Both cohorts were divided into quartiles according to cystatin C at entry. In the non-AKI cohort, we split the highest cystatin C quartile into two. The relationship between the different cystatin C quartiles and mortality in patients with and without AKI was estimated by hazard ratios (HR) derived from the Cox proportional hazards regression model. RESULTS: A relationship between cystatin C and mortality was found in patients with and without AKI, being stronger in patients without AKI. In AKI patients, the HR comparing cystatin C above and below the median more than doubled from the second year on compared to the first year follow-up. After exclusion of patients in the non-AKI cohort with 'potential AKI' (creatinine >100 micromol/l or urea > 20 mmol/l), the correlation between cystatin C levels and risk of death was strengthened. CONCLUSIONS: Cystatin C is correlated with mortality independently of renal function measured by creatinine in patients entering the general ICU.

End-stage renal disease patients on renal replacement therapy in the intensive care unit: short- and long-term outcome.

OBJECTIVE: The number of patients with end-stage renal disease has increased during the last decades. Data shows that 10% of the renal replacement therapy population in the intensive care unit are patients with end-stage renal disease. We aimed to describe the short- and long-term outcome of these patients after renal replacement therapy in the intensive care unit. DESIGN: Nationwide cohort study between the years 1995 and 2004. Follow-up up to 5 years. SETTING: Swedish general intensive care units and Swedish hospitals. PATIENTS: Eligible subjects were end-stage renal disease patients treated with renal replacement therapy in 32 Swedish general intensive care units. In total, 245 patients were studied. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Short- and long-term mortality was studied. Logistic regression was used to analyze short-term mortality. Long-term mortality was compared with the mortality of end-stage renal disease patients outside the intensive care unit and the mortality in the population. Diabetes and heart failure are significant risk factors for 90-day mortality, with an odds ratio of 1.9 and 2.0, respectively. The intensive care unit end-stage renal disease cohort had increased long-term mortality as compared with non-intensive care unit end-stage renal disease patients, relative risk of death 2.32 (confidence interval 1.84-2.92). A comparison with the mortality rate in the general population yielded a standardized mortality ratio of 25 (95% confidence interval: 19.6-31.4). CONCLUSIONS: For end-stage renal disease patients in the intensive care unit, age, diabetes mellitus, and heart failure are risk factors for 90-day mortality. Long-term mortality is associated with age and heart failure. The long-term mortality of end-stage renal disease patients surviving the intensive care unit stay is significantly higher compared with end-stage renal disease patients without a known intensive care unit admission.

Effect of bicarbonate on muscle protein in patients receiving hemodialysis.

BACKGROUND: Metabolic acidosis stimulates whole-body net protein breakdown in healthy adults and patients with kidney failure, but few studies investigated how acidosis affects protein metabolism in individual tissues, such as skeletal muscle. METHODS: We evaluated the effect of metabolic acidosis on protein turnover in skeletal muscle, assessed by means of phenylalanine kinetics and free amino acid concentrations in plasma and muscle. Long-term hemodialysis patients (n = 16) were divided into 2 groups in an open crossover study design. In group A, we administered bicarbonate supplements and increased blood standard bicarbonate levels from 17.8 +/- 0.03 to 27.1 +/- 1.2 mEq/L (17.8 +/- 0.03 to 27.1 +/- 1.2 mmol/L). In group B, we decreased bicarbonate supplements, which caused a decrease in standard bicarbonate levels from 26.6 +/- 0.7 to 18.6 +/- 0.3 mEq/L (26.6 +/- 0.7 to 18.6 +/- 0.3 mmol/L). RESULTS: Net phenylalanine efflux from leg tissues (muscle) was significantly less when acid-base balance was corrected compared with acidosis (10.8 +/- 1.5 versus 18.6 +/- 3.8 nmol/min/100 g tissue; P = 0.014), as was the rate of phenylalanine appearance (28.3 +/- 3.0 versus 38.4 +/- 5.9 nmol/min/100 g tissue; P = 0.016); the rate of phenylalanine disposal was unchanged. Cortisol and C-reactive protein levels in blood were unchanged after correction of acidosis, as were levels of messenger RNAs encoding components of the ubiquitin-proteasome pathway in muscle biopsy specimens. CONCLUSION: Our findings indicate that acidosis increases protein breakdown in skeletal muscle, but additional studies are needed to identify the pathways stimulated to degrade muscle protein in response to acidosis.

Changes in right ventricular pressures between hemodialysis sessions recorded by an implantable hemodynamic monitor.

Intermittent and chronic volume overload might contribute to the onset and progression of cardiovascular disease in patients who are undergoing maintenance hemodialysis (HD). Continuous monitoring of central hemodynamic variables may provide valuable information to improve volume control, particularly in patients with left ventricular dysfunction. Sixteen patients with end-stage renal disease who were undergoing long-term HD received an implantable hemodynamic monitor consisting of a subcutaneously implanted memory device and transvenous right ventricular (RV) lead with a pressure sensor. The implantable hemodynamic monitor continuously records heart rate, RV pressures, and estimated pulmonary arterial (PA) diastolic pressure, an estimate of left ventricular filling pressure. All patients underwent HD 3 times per week, and averages of rest hemodynamic values from the first, second, and third nights after HD during 12 weeks were analyzed. The third night always occurred after the weekend, when there was an extended interval between dialysis sessions. From the first night to the second night, RV systolic pressure increased by 10 +/- 8% (p <0.001), and estimated PA diastolic pressure increased by 16 +/- 14% (p <0.001). On the third night, RV systolic pressure increased by 14 +/- 12% (p <0.001), and estimated PA diastolic pressure increased by 23 +/- 18% (p <0.001) compared with the first night. In conclusion, the progressive pressure increments between dialysis sessions seen in this study suggest that the implantable hemodynamic monitor was a sensitive indicator for changes in volume load in patients who were undergoing HD treatment. The results also suggest that more frequent dialysis may avoid excessive pressure increase, but this needs to be investigated further in future studies.